Posts made by Lejeboca

@Mauritio
As a rule of thumb, you need more quantity of a plant as food than as an extract to achieve the same effects.
What horseradish you eat as food is on the order of grams for a single serving, I imagine, while 1-3 drops contain less than a milligram of the plant matter.

With extracts, it is easier to gauge the dosage too.

I, personally, like alcohol extracts because they are stored for a long time and are always on hand. A 30ml bottle would last for 8 months to a year in the dosage as above.

Cross-linking here my post about horseradish inhibiting tumor-cell proliferation which I posed in the Cancer tread here:

https://bioenergetic.forum/post/24447

Again small doses of extract components seemed to be used.

Stumbled on this one from references in links in the Horseradish thread but didn't read beyond the abstract.

Tumor cell proliferation and cyclooxygenase inhibitory constituents in horseradish (Armoracia rusticana) and Wasabi (Wasabia japonica)

Abstract

Cyclooxygenase and human tumor cell growth inhibitory extracts of horseradish (Armoracia rusticana) and wasabi (Wasabia japonica) rhizomes upon purification yielded active compounds 1-3 from horseradish and 4 and 5 from wasabi rhizomes. Spectroscopic analyses confirmed the identities of these active compounds as plastoquinone-9 (1), 6-O-acyl-beta-d-glucosyl-beta-sitosterol (2), 1,2-dilinolenoyl-3-galactosylglycerol (3), linolenoyloleoyl-3-beta-galactosylglycerol (4), and 1,2-dipalmitoyl-3-beta-galactosylglycerol (5). 3-Acyl-sitosterols, sinigrin, gluconasturtiin, and phosphatidylcholines isolated from horseradish and alpha-tocopherol and ubiquinone-10 from wasabi rhizomes isolated were inactive in our assays. At a concentration of 60 microg/mL, compounds 1 and 2 selectively inhibited COX-1 enzyme by 28 and 32%, respectively. Compounds 3, 4, and 5 gave 75, 42, and 47% inhibition of COX-1 enzyme, respectively, at a concentration of 250 microg/mL. In a dose response study, compound 3 inhibited the proliferation of colon cancer cells (HCT-116) by 21.9, 42.9, 51.2, and 68.4% and lung cancer cells (NCI-H460) by 30, 39, 44, and 71% at concentrations of 7.5, 15, 30, and 60 microg/mL, respectively. At a concentration of 60 microg/mL, compound 4 inhibited the growth of colon, lung, and stomach cancer cells by 28, 17, and 44%, respectively. This is the first report of the COX-1 enzyme and cancer cell growth inhibitory monogalactosyl diacylglycerides from wasabi and horseradish rhizomes.

@Amazoniac Thanks!
It is on my reading list now! Main goal not to side-track

@Mauritio Thanks for posting and renewing our attention to horseradish!

Eating is good (clears out sinuses, anti-bacterial, etc.)

The 1st paper you've referenced, however, considers the extract for "LPS-induced inflammation in macrophages" to concentrate the acting agents, I suppose "allyl-isothiocyanate (AITC) effects, its main ITC resulting from the hydrolysis of the corresponding glucosinolate sinigrin by myrosinase enzyme".

So, indeed very small dose is needed (the highest dilution of the extract was 1/5th) to achieve the effects. The powder extract itself was prepared in a rather standard lab way. I am surprised though how weak it is:
10g:100ml | material (freeze-dried root) to alcohol ratio.

All in all, I think making a simple horseradish alcohol tincture and using it in 1-3 drop doses will be close to the study in terms of effects on LPS-induced inflammation.

Specifically: Take 20g of horseradish (middle of the) root, wash, finely chop, put into a glass jar, add 40ml of the highest proof alcohol you can find but no less than 100 proof. Cover with lid tightly and let sit in a dark place for 2-3 weeks or more. Shake from time to time. Strain (decant) and -- voilà -- the strained liquid is your horseradish tincture.

It looks like the study pre-treated cells with the dilution for 1h and then exposed to LPS for 24 hours before measurements. Based on this, as preventative, I'd take 1-3 drops of the tincture in a bit of water 1x per day.

From:
Inducible nitric oxide synthase: what difference does it make?

"The [iNOS} dichotomy is sometimes manifest at different times or sites in the same experimental setting."

"In both infection and inflammation, iNOS appears to act both as a direct effector and as a regulator of other effectors."

"..the cytotoxic and proinflammatory potential of iNOS advances the case for its therapeutic inhibition in those of the diseases discussed above that are not thought to be infectious in etiology, such as Alzheimer’s disease, hemorrhagic shock/resuscitation, late-phase vasoocclusive stroke, inflammatory bowel disease, and rheumatoid and osteoarthritis, or in those infectious diseases where the inflammatory effect of iNOS appears to outweigh its antimicrobial effect, such as influenza pneumonia. However, the antiinflammatory role of iNOS emphasizes the possibility of adverse consequences attendant on its inhibition."

@wtpyrucet , There are quite a few posts on RPF related to comfrey and its high content of allantoin.
For example here is an interesting post:

Title: what-hormones-are-involed-in-penis-growth-size.18417
Post number: 43
Author: TreasureVibe
Date: May 15, 2019 at 2:05 AM

"Post by me from another topic, posting in here because this topic seems more relevant: What do you guys think of this? There is a substance in Comfrey Root and Plantain called "Allantoin" which research shows accelerates cellular mitosis, which means it grows new tissue growth: "As some of its other names suggest, (knitbone, boneset) Comfrey has been prized since ancient times for its ability to help heal broken bones and damaged tissues. In modern times, it has been discovered that this is at least in part due to a substance in Comfrey called ‘allantoin’ that is able to accelerate cellular 'mitosis', meaning it speeds the process of new tissue growth." Richard Whelan ~ Medical Herbalist ~ Comfrey Root "~ Plantain has several active ingredients that contribute to its medicinal action; allantoin, a substance that is well proven to stimulate tissue regeneration through causing cells to divide more vigorously (via mitosis), aucubin, a substance with proven antibiotic actions and mucilage, a soothing, natural anti-inflammatory substance." Richard Whelan ~ Medical Herbalist ~ Plantain"

To add on to the 'diet' discussion here, I quote Travis' post from RPF, on which I stumbled again just now while searching the archives:

Tite : treatments-with-tumor-dissolving-potential.15301
Post #: 4
Author: Travis
Date: Nov 9, 2017 at 10:38 AM

"Pau d'Arco has the most powerful natural glyoxylase I inhibitors known: lapachol and β-lapachone. There's been dozens of studies on these two molecules, which tie-in nicely with the work of Koch and Szent-Györgyi. I would put this plant at the very top of the list, although curcumin should be the best for lower GI cancers since it basically coats the intestines. There's been a few pharmacokinetic studies demonstrating how curcumin is distributed within the body. The amino acid L-threonine will become methylglyoxal within the body (through aminoacetone intermediate), so pau d'arco with L-threonine would appear to be a safe and all-natural Szent-Györgyi-approved approach—with a Koch Seal of Approval—to raise intracellular methylglyoxal levels. Add to this a Gerson-type diet (sans the linoleic acid-containing flaxseed oil) and you'd probably be reversing tumors in a manner similar to the lab-rats given such things. Glyoxylase I & II together turn methylglyoxal into lactic acid. Inhibiting one of these enzymes lowers intracellular lactic acid concentrations. Considering just this one enzymatic system alone, low methylglyoxal levels are synonymous with high lactic acid levels. This could help explain the findings of Otto Warburg, while linking together the apparently unrelated observations of two great biochemical Nobelists—Otto Warburg of Germany and Albert Szent-Györgyi of Hungary. The plant polyphenol baicalein appears to the most powerful glyoxylase I inhibitor among the class of polyphenols. The low-methionine diet of Gerson should be stressed, as is low in methionine; this would be expected to lead to low intracellular polyamine levels—powerful growth factors which act on DNA replication by directly stabilizing and/or uncoiling the helix. Methylglyoxal binds to, and inactivates polyamines. And limiting linoleic acid should limit excessive prostaglandins, intracellular autocrine hormones which effect DNA→mRNA transcription through the nuclear PPAR receptors."

Digging a bit deeper into refs 8 and 26 in my post above.

(8) UV radiation suppresses experimental autoimmune encephalomyelitis independent of vitamin D production
by Bryan R Becklund , Kyle S Severson, Souriya V Vang, Hector F DeLuca

From the abstract:

Our results indicate that continuous treatment with UVR dramatically suppresses clinical signs of [the experimental autoimmune encephalomyelitis] EAE. Interestingly, disease suppression occurs with only a modest, transient increase in serum 25(OH)D(3) levels. Further analysis demonstrated that the levels of 25(OH)D(3) obtained upon UVR treatment were insufficient to suppress EAE independent of UVR treatment. These results suggest that UVR is likely suppressing disease independent of vitamin D production, and that vitamin D supplementation alone may not replace the ability of sunlight to reduce MS susceptibility.

(26) Suppression of experimental autoimmune encephalomyelitis by ultraviolet light is not mediated by isomerization of urocanic acid
by Amy A. Irving, Steven J. Marling, Lori A. Plum, and Hector F. DeLuca

From the Discussion:

It is clear that ultraviolet B exposure efficiently prevents EAE, though we find no evidence to support [urocanic acid] UCA isomerization as the mediator of this suppression. This is not the first study to discount UCA as a mediator of UV immunosuppression, or that UCA administration does not mimic the effects of UV exposure.

@Amazoniac, Super interesting. Thanks for the find.

Inspired me to learn a bit about S1P.

• The sphingosine-1-phosphate (S1P) is very important for immune suppression and cell proliferation via its receptor 1 (S1PR1) :
  "..S1PR1 is crucial for S1P-induced cell migration and suggested that S1PR1 is a master regulator of cell movement", as was shown in this work."

How clever: UVR modulates the systemic immune system via this global mechanism (S1PR1) and not via vitamin D (8) or urocanic acid (26), which I reckon would be more indirect solutions than the S1PR1 one.
[Reference number 8 and 26 are taken the paper in the OP.]

@Amazoniac said in cancer:

It must be best for the methionine restriction to affect its concentration in circulation (or else cells keep acquiring it) and to moderate the one-carbon donors that promote its regeneration.

Methionine restriction may also potentialize the effects of radiation- and chemo-therapies:

Methionine diet restriction both inhibits tumor growth and radiosensitizes RAS-driven sarcoma models [65,66]. Methionine restriction also improves the efficacy of chemotherapeutic drugs. For example, in tumor-bearing rats, depleting methionine increased the efficacy of vincristine [67].

From Interactions between Radiation and One-Carbon Metabolism, a review paper published in Int J Mol Sci. 2022 Feb 8;23(3):1919.

@Jennifer

@Kasper, why do you think so?

I also don't think Ray Peat inspired diets are gonna fix this, but actually could make it worse

Also, could you please provide a pubmed or other 'official' site link?
The sub-hub.se doesn't display on all browsers/set-ups equally well.
(I get a blank page, e.g.)
Thank you

In the US, American elderberry (Sambucus canadensis) is more prevalent than the European (black) elderberry (Sambucus nigra).

S. canadensis "individuals ranged nearly threefold from 1308 to 4004 µg [of cyanidin 3-glucoside equivalents] (cy3-GE)/g on a fresh weight basis" per this paper that assesses 14 different varieties in the US.
Total phenolic, anthocyanin contents and antioxidant capacity of selected elderberry (Sambucus canadensis L.) accessions

Comparing the two species of elderberry in a metanalysis, the following paper concludes this about their composition:
"The most abundant type of anthocyanidin in the European and the American elderberries is cyanidin. In S. nigra, the anthocyanins are not acylated, while in S. canadensis the major individual anthocyanins are acylated with E-p-coumaroyl functionality at C-3. Acylation was reported to stabilize anthocyanins against heat and light. However, glycosidation was observed to improve the stability of anthocyanins against light, but not against heat. Despite the structural variation of the anthocyanins—-represented by a number of hydroxyl groups and the substitution of hydroxyl groups with methoxyl groups, as well as the type and number of sugar residues attached to the flavylium cation via glycosidic linkages—the literature reveals that the anthocyanins of different cultivars of elderberry share several pharmacological effects."
Elderberry Extracts: Characterization of the Polyphenolic Chemical Composition, Quality Consistency, Safety, Adulteration, and Attenuation of Oxidative Stress- and Inflammation-Induced Health Disorders

Seems like hemp was a minority ingredient in the formula (1g vs 5 g of menthol and 600g of peppermint oil).
This is probably due to their stipulation that "The effects of CBD on hair growth are dose dependent and higher doses may result in premature entry into the catagen phase through a different receptor known as TRPV4."

Furthermore, the authors conclude that "Although the exact mechanism of therapeutic effects is not entirely clear, CBD is most likely functioning as a CB1 receptor antagonist, through negative allosteric effects, and potentially also through Wnt messaging. THCV and CBDV are acting as full CB1 neutral antagonists and through TRPV1 agonism. The menthol and peppermint (40% menthol) are probably acting by promoting the rapid onset of anagen phase.[1]"

N.B. While hemp helps to maintain anagen (i.e., growth) phase, first you need to start it. I'd say menthol would be more effective for hair growth than based on the above.

[1] Peppermint Oil Promotes Hair Growth without Toxic Signs

@Fructose said in Chamomile has anti-estrogen and pro-progesterone properties:

his plant can function as a selective estrogen receptor, and this property can be harnessed in regulating endogenous estrogens in individuals with PCOS who have high estrogen levels.

A detailed study showing the selective estrogen receptor modulator (SERM) properties of chamomille:

Greek Plant Extracts Exhibit Selective Estrogen Receptor Modulator (SERM)-like Properties

From the abstract: "...we submitted four plant aqueous extracts derived from
Greek flora (Sideritis euboea, Sideritis clandestina, Marticaria chamomilla, and Pimpinella anisum)
in a series of in vitro biological assays reflective of SERM profile. We examined their ability (a) to
stimulate the differentiation and mineralization of osteoblastic cell culture by histochemical staining
for alkaline phosphatase and Alizarin Red-S staining, (b) to induce, like antiestrogens, the insulin
growth factor binding protein 3 (IGFBP3) in MCF-7 breast cancer cells, and (c) to proliferate cervical
adenocarcinoma (HeLa) cells by use of MTT assay.

From Discussion:
(a) "Our study therefore, based on reliable biological tests and biochemical markers reflective of osteoblastic activity, reveals that the aqueous extracts of Sideritis euboea, Sideritis clandestina, Marticaria chamomilla, and Pimpinella anisum stimulated differentiation and mineralization significantly at a concentration range 50-25 µg/mL."

(b) "The antiestrogenic effect of plant extracts on IGFBP3 levels was observed at a concentration of 10 µg/mL, whereas at higher concentrations (25-50 µg/mL), there was no effect. This is in agreement with previous reports, which demonstrate that plant extracts may exhibit differential activities over a physiological concentration range (being agonist or antagonist) suggesting an estrogen-receptor-mediated effect at low concentration and an ER-independent effect at higher concentration."

(c) "The absence of proliferative effects of the extracts on HeLa cells implicates that their action is neutral on these cells, at least via an EBS type II dependent mechanism."

@Kasper said:

Isn't that caused by apigenin?

"In our experiments, we cannot attribute the biological effects observed to particular constituents, because many other compounds are present in the plant extracts. Our study investigates the effect of the plant aqueous extracts as a whole on bone metabolism, as well as on breast and uterine tumor cells."

@Amazoniac ,
Good catch. Thanks for the correction. I've edited my post (the 1st two bullets).
I am a bit puzzled though why the authors in the OP study didn't use monomeric Si if they were looking for Si bioavailability. Perhaps, the concentrations of the Si polymer that they fed to the rats were low enough that they formed monomers...

@Amazoniac

• Interesting find -- thank you -- especially in conjunction with the other Si benefits we've considered and discussions on which forms of Si are bioavailable and which are not, such as in Oligomeric but not monomeric silica prevents aluminum absorption in humans - PubMed

• The authors in the OP paper do not discuss their choice of Si but directly take the polymeric form, sodium metasilicate, which is less bioavailable according to the paper mentioned in my bullet item above. However, the rate of bioavailability seems to depend on the dilution of the concentrated silica solutions, in which case "the formation of monomeric silica is likely".

• Good to know also that "The physiological amounts of dietary silicon, compared to inadequate silicon, in the present experiment increased the activity of an enzyme necessary for collagen formation, enhanced collagen deposition" and that these amounts apparently met by commercial rat diet.

• Side note: Authors also speculate that to see an effect on Ca levels a longer supplementation might be needed:
  This is in contrast to findings obtained in other experiments by us (9). The difference, however, probably was related to the age of the animals or the length of time the animals were maintained on the silicon-deficient diet. In previous experiments, weanling rats were fed the silicon-deficient diet for 8 or 9 wk before bones were obtained for analysis; in the present experiment, weanling rats were fed the silicon-deficient diets for only 3 wk."

• • Interesting that the effect on collagen is seen much earlier than that on calcium.

Hi @Mauritio ,
100% agree and it feels good to be here. I will be reposting my RPF stuff here too.
Thank you @brad for creating this space!